• Publication type
• Meeting Abstract MeSH

Despite the recent progress in research and therapy, cardiovascular diseases are still the most common cause of death worldwide, thus new approaches are still needed. The aim of this review is to highlight the cardioprotective potential of urocortins and corticotropin-releasing hormone (CRH) and their signaling. It has been documented that urocortins and CRH reduce ischemic and reperfusion (I/R) injury, prevent reperfusion ventricular tachycardia and fibrillation, and improve cardiac contractility during reperfusion. Urocortin-induced increase in cardiac tolerance to I/R depends mainly on the activation of corticotropin-releasing hormone receptor-2 (CRHR2) and its downstream pathways including tyrosine kinase Src, protein kinase A and C (PKA, PKCε) and extracellular signal-regulated kinase (ERK1/2). It was discussed the possibility of the involvement of interleukin-6, Janus kinase-2 and signal transducer and activator of transcription 3 (STAT3) and microRNAs in the cardioprotective effect of urocortins. Additionally, phospholipase-A2 inhibition, mitochondrial permeability transition pore (MPT-pore) blockade and suppression of apoptosis are involved in urocortin-elicited cardioprotection. Chronic administration of urocortin-2 prevents the development of postinfarction cardiac remodeling. Urocortin possesses vasoprotective and vasodilator effect; the former is mediated by PKC activation and prevents an impairment of endothelium-dependent coronary vasodilation after I/R in the isolated heart, while the latter includes both cAMP and cGMP signaling and its downstream targets. As CRHR2 is expressed by both cardiomyocytes and vascular endothelial cells. Urocortins mediate both endothelium-dependent and -independent relaxation of coronary arteries.

• MeSH
• Corticotropin-Releasing Hormone pharmacology   MeSH
• Hormones pharmacology   MeSH
• Cardiovascular Physiological Phenomena drug effects   MeSH
• Cardiovascular Diseases drug therapy   MeSH
• Cardiovascular System drug effects   MeSH
• Rats MeSH
• Humans MeSH
• Reperfusion Injury drug therapy   MeSH
• Urocortins pharmacology   MeSH
• Vasodilation drug effects   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH

Publikace se zaměřuje na diagnostiku a léčbu nemocí endokrinního systému. Určeno odborné veřejnosti.; Přehled pro lékaře, kteří nejsou endokrinology či diabetology, o možných endokrinologických onemocněních.

• MeSH
• Diagnostic Techniques, Endocrine MeSH
• Endocrine System Diseases diagnosis   therapy   MeSH
• Publication type
• Monograph MeSH

• Conspectus
• Fyziologie člověka a srovnávací fyziologie
• NML Fields
• endokrinologie

Chronic stress is a crucial public issue that occurs when a person is repetitively stimulated by various stressors. Previous researches have reported that chronic stress induces spermatogenesis dysfunction in the reproductive system, but its molecular mechanisms remain unclear. The nectin protein family, including nectin-1 to nectin-4, is Ca(2+)-independent immunoglobulin-like cell adhesion molecules, that are widely expressed in the hippocampus, testicular tissue, epithelial cells and other sites. Nectin-3 contributes to the sperm development at the late stage, and the abnormal expression of nectin-3 impairs spermatogenesis. Some recent studies have demonstrated that stress induces a decrease in nectin-3 expression in the hippocampus via corticotropin-releasing hormone (CRH) to corticotropin-releasing hormone receptor 1 (CRHR1) pathway. Here, we tested whether chronic stress also caused a reduction in nectin-3 expression in the testis. We established a chronic social defeat stress paradigm, which provides naturalistic and complex chronic stress inmale C57BL/6 mice. After 25 days of chronic social defeat stress, the mice showed weight loss, thymic atrophy and some other typical symptoms of chronic stress (e.g.anxiety-like behavior and social avoidance behavior). We found gonad atrophy, testicular histological structure changes and semen quality reductions in the stressed mice. The stressed male mice significantly spent more time to impregnate the female mice than the control male mice. Moreover, nectin-3 protein levels in stressed mice were significantly decreased in the testes compared with those in control mice. In addition, we found that the CRHR1 expression level was increased in the testes of stressed mice. Therefore, we demonstrated a decreased level of nectin-3 expression and an increase in CRHR1 expression in the testis after exposure to chronic stress, which may provide a potential therapeutic target for the spermatogenesis dysfunction induced by chronic stress.

• MeSH
• Mice, Inbred C57BL MeSH
• Mice MeSH
• Nectins biosynthesis   MeSH
• Stress, Psychological metabolism   physiopathology   MeSH
• Receptors, Corticotropin-Releasing Hormone biosynthesis   metabolism   MeSH
• Social Interaction MeSH
• Spermatogenesis physiology   MeSH
• Testis metabolism   physiopathology   MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

The gut microbiota play an important role in shaping brain functions and behavior, including the activity of the hypothalamus-pituitary-adrenocortical (HPA) axis. However, little is known about the effect of the microbiota on the distinct structures (hypothalamus, pituitary, and adrenals) of the HPA axis. In the present study, we analyzed the influence of the microbiota on acute restraint stress (ARS) response in the pituitary, adrenal gland, and intestine, an organ of extra-adrenal glucocorticoid synthesis. Using specific pathogen-free (SPF) and germ-free (GF) male BALB/c mice, we showed that the plasma corticosterone response to ARS was higher in GF than in SPF mice. In the pituitary, stress downregulated the expression of the gene encoding CRH receptor type 1 (Crhr1), upregulated the expression of the Fkbp5 gene regulating glucocorticoid receptor sensitivity and did not affect the expression of the proopiomelanocortin (Pomc) and glucocorticoid receptor (Gr) genes. In contrast, the microbiota downregulated the expression of pituitary Pomc and Crhr1 but had no effect on Fkbp5 and Gr. In the adrenals, the steroidogenic pathway was strongly stimulated by ARS at the level of the steroidogenic transcriptional regulator Sf-1, cholesterol transporter Star and Cyp11a1, the first enzyme of steroidogenic pathway. In contrast, the effect of the microbiota was significantly detected at the level of genes encoding steroidogenic enzymes but not at the level of Sf-1 and Star. Unlike adrenal Sf-1, the expression of the gene Lrh-1, which encodes the crucial transcriptional regulator of intestinal steroidogenesis, was modulated by the microbiota and ARS and this effect differed between the ileum and colon. The findings demonstrate that gut microbiota have an impact on the response of the pituitary, adrenals and intestine to ARS and that the interaction between stress and the microbiota during activation of glucocorticoid steroidogenesis differs between organs. The results suggest that downregulated expression of pituitary Pomc and Crhr1 in SPF animals might be an important factor in the exaggerated HPA response of GF mice to stress.

• MeSH
• Cholesterol Side-Chain Cleavage Enzyme genetics   MeSH
• Phosphoproteins genetics   MeSH
• Restraint, Physical * MeSH
• Pituitary Gland metabolism   MeSH
• Ileum metabolism   microbiology   MeSH
• Colon metabolism   microbiology   MeSH
• Corticosterone blood   MeSH
• Mice, Inbred BALB C MeSH
• Adrenal Glands metabolism   MeSH
• Pro-Opiomelanocortin genetics   MeSH
• Stress, Psychological blood   microbiology   MeSH
• Receptors, Corticotropin-Releasing Hormone genetics   MeSH
• Gene Expression Regulation MeSH
• Steroidogenic Factor 1 genetics   MeSH
• Gastrointestinal Microbiome * MeSH
• Pituitary-Adrenal System * MeSH
• Hypothalamo-Hypophyseal System * MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Učebnice je koncipována jako výchozí text pro pregraduální výuku gynekologie a obsahuje základy všech jejích podoborů.; Odborná publikace určená studentům medicíny, výchozí text pro pregraduální výuku gynekologie.

• MeSH
• Genital Diseases, Female MeSH
• Gynecologic Surgical Procedures MeSH
• Gynecological Examination MeSH
• Infertility MeSH
• Genitalia, Female abnormalities   anatomy & histology   physiology   MeSH

• Conspectus
• Gynekologie. Porodnictví
• Učební osnovy. Vyučovací předměty. Učebnice
• NML Fields
• gynekologie a porodnictví
• NML Publication type
• kolektivní monografie
• učebnice vysokých škol

Mateřská deprese je jednou z nejčastějších prenatálních a postnatálních komplikací. Takové komplikace mohou vážně ohrozit neuropsychický vývoj nového jedince. Článek poskytuje přehled možných biologických, neurologických a psychologických faktorů, které mohou být zahrnuty mezi faktory rizikové. Perinatální deprese matky je prezentována a diskutována jako příklad interakce placentárních, epigenetických a raných rodičovských faktorů, které zvyšují riziko narušení vývoje plodu, novorozence, kojence a dítěte v dalších věkových obdobích. Dostupné důkazy poukazují na důležitost vlivů, které působí na jedince již v děloze matky, stejně jako na význam časné citové vazby a mateřské péče. Je zřejmé, že modely rané etiologie duševních poruch, jakou je i perinatální deprese, jsou složité s řadou potenciálních faktorů od genetických a epigenetických až po faktory prostředí, jež ovlivňují neurologický, emoční a psychosociální vývoj.

Maternal depression is one of the most common prenatal and postnatal complications. Such complications may seriously compromised the neuropsychological development of the new being. This paper provides an overview of potential biological, neurological and psychological factors that might be involved into the risk factors. Perinatal maternal depression is presented and reviewed as an example of the interaction of placental, epigenetic and early parenting factors elevating risk of poor fetus, neonatal, infant and child development. Available evidence points to the importance of in-utero influences as well as the importance of early attachment and parenting. It is pointed out that models of the early aetiology of mental disorders, such as perinatal depression, are complex with a range of potential factors from genetic and epigenetic to environmental influencing neurological, emotional and psychosocial development.

• Keywords
• citlivost,
• MeSH
• Central Nervous System physiology   growth & development   MeSH
• Depression * epidemiology   etiology   genetics   psychology   MeSH
• Epigenesis, Genetic physiology   MeSH
• Corticotropin-Releasing Hormone physiology   MeSH
• Gene-Environment Interaction MeSH
• Humans MeSH
• Infant, Newborn MeSH
• Peripartum Period physiology   genetics   psychology   MeSH
• Placenta physiology   MeSH
• Object Attachment MeSH
• Parenting psychology   MeSH
• Social Interaction MeSH
• Pregnancy MeSH
• Child Development * MeSH
• Check Tag
• Humans MeSH
• Infant, Newborn MeSH
• Pregnancy MeSH
• Female MeSH
• Publication type
• Review MeSH

• MeSH
• Galanin physiology   MeSH
• Gastrointestinal Hormones physiology   MeSH
• Gonadotropin-Releasing Hormone analysis   metabolism   MeSH
• Corticotropin-Releasing Hormone analysis   metabolism   MeSH
• Hypothalamus physiology   metabolism   MeSH
• Insulin physiology   metabolism   MeSH
• Leptin analysis   metabolism   MeSH
• Humans MeSH
• Anorexia Nervosa metabolism   physiopathology   MeSH
• Neuropeptide Y physiology   MeSH
• Neurosecretory Systems physiology   physiopathology   MeSH
• Obesity etiology   metabolism   physiopathology   MeSH
• Orexins physiology   metabolism   MeSH
• Feeding and Eating Disorders etiology   metabolism   physiopathology   MeSH
• Appetite Regulation physiology   MeSH
• Hypothalamo-Hypophyseal System physiopathology   MeSH
• Adipose Tissue chemistry   metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH

The activation of the HPA axis is the endocrine measure of stress responsiveness that is initiated by corticotropin-releasing hormone (CRH). CRH exerts its effects via CRHR1 and CRH-R2 receptors coupled to the cAMP signaling system and this process involves transcription factor cAMP-responsive element-binding protein (CREB).This study investigated the role of CRH and the possible involvement of CREB in gene regulation of CRH receptor, under basal conditions and after stress application in the pituitary. We used wild type (wt +/+) controls and CRH knock-out (CRH-KO -/-) male mice. Using CRH-deficient mice, we were able to investigate the consequences of the lack of the CRH on the expression of CRH receptors and transcriptional regulation mediated by CREB. We estimated the effect of acute (IMO 1×) and repeated (IMO 7×) restraint stressors lasting 30 and 120 min on the expression of mRNA CREB, CRH-R1, and CRH-R2 by qPCR. We found very significant difference in the expression of these peptides under the effect of single and repeated stress in control and CRH-KO mice. Our results indicate that both CRH receptors and CREB might be involved in the regulation of stress response in the pituitary of mice. We propose that regulation of the stress response may be better understood if more were known about the mechanisms of CRH receptor signal transduction and involvement of CREB system.

• MeSH
• Acute Disease MeSH
• Corticotropin-Releasing Hormone biosynthesis   deficiency   MeSH
• Pituitary Gland metabolism   MeSH
• Mice, Inbred C57BL MeSH
• Mice, Knockout MeSH
• Mice MeSH
• Cyclic AMP Response Element-Binding Protein biosynthesis   MeSH
• Stress, Psychological metabolism   psychology   MeSH
• Receptors, Corticotropin-Releasing Hormone biosynthesis   MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

The commensal microbiota affects brain functioning, emotional behavior and ACTH and corticosterone responses to acute stress. However, little is known about the role of the microbiota in shaping the chronic stress response in the peripheral components of the hypothalamus-pituitary-adrenocortical (HPA) axis and in the colon. Here, we studied the effects of the chronic stress-microbiota interaction on HPA axis activity and on the expression of colonic corticotropin-releasing hormone (CRH) system, cytokines and 11β-hydroxysteroid dehydrogenase type 1 (11HSD1), an enzyme that determines locally produced glucocorticoids. Using specific pathogen-free (SPF) and germ-free (GF) BALB/c mice, we showed that the microbiota modulates emotional behavior in social conflicts and the response of the HPA axis, colon and mesenteric lymph nodes (MLN) to chronic psychosocial stress. In the pituitary gland, microbiota attenuated the expression of Fkbp5, a gene regulating glucocorticoid receptor sensitivity, while in the adrenal gland, it attenuated the expression of genes encoding steroidogenesis (MC2R, StaR, Cyp11a1) and catecholamine synthesis (TH, PNMT). The pituitary expression of CRH receptor type 1 (CRHR1) and of proopiomelanocortin was not influenced by microbiota. In the colon, the microbiota attenuated the expression of 11HSD1, CRH, urocortin UCN2 and its receptor, CRHR2, but potentiated the expression of cytokines TNFα, IFNγ, IL-4, IL-5, IL-6, IL-10, IL-13 and IL-17, with the exception of IL-1β. Compared to GF mice, chronic stress upregulated in SPF animals the expression of pituitary Fkbp5 and colonic CRH and UCN2 and downregulated the expression of colonic cytokines. Differences in the stress responses of both GF and SPF animals were also observed when immunophenotype of MLN cells and their secretion of cytokines were analyzed. The data suggest that the presence of microbiota/intestinal commensals plays an important role in shaping the response of peripheral tissues to stress and indicates possible pathways by which the environment can interact with glucocorticoid signaling.

• MeSH
• 11-beta-Hydroxysteroid Dehydrogenase Type 1 metabolism   MeSH
• Adrenocorticotropic Hormone metabolism   MeSH
• Behavior, Animal physiology   MeSH
• Cytokines metabolism   MeSH
• Gene Expression physiology   MeSH
• Glucocorticoids genetics   physiology   MeSH
• Corticotropin-Releasing Hormone metabolism   MeSH
• Pituitary Gland MeSH
• Corticosterone metabolism   MeSH
• Microbiota physiology   MeSH
• Mice, Inbred BALB C MeSH
• Mice MeSH
• Adrenal Glands MeSH
• Stress, Psychological genetics   metabolism   MeSH
• Psychology MeSH
• Receptors, Glucocorticoid metabolism   MeSH
• Gene Expression Regulation physiology   MeSH
• Social Behavior MeSH
• Pituitary-Adrenal System microbiology   MeSH
• Hypothalamo-Hypophyseal System microbiology   MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH